Acute effects of casein on postprandial lipemia and incretin responses in type 2 diabetic subjects

Lea Johanne Brader, L. Holm, L. Mortensen, C. Thomsen, Arne Astrup, Jens Juul Holst, M. de Vrese, J. Schrezenmeir, Kjeld Hermansen

20 Citationer (Scopus)

Abstract

Background and aims: Exaggerated and prolonged postprandial lipemia is potentially atherogenic and associated with type 2 diabetes. Limited data exist regarding the influence of dietary protein on postprandial lipemia in type 2 diabetes. We investigated, over 8-h, the acute effects of casein alone or in combination with carbohydrate on postprandial lipid and incretin responses to a fat-rich meal in type 2 diabetes. Methods and results: Eleven type 2 diabetic subjects ingested four test meals in random order: an energy-free soup plus 80 g of fat (control-meal); control-meal plus 45 g carbohydrates (CHO-meal); control-meal plus 45 g of casein (PRO-meal); and PRO-meal plus 45 g carbohydrates (CHO + PRO-meal). Triglyceride and retinyl palmitate responses were measured in plasma and in a chylomicron-rich and chylomicron-poor fraction. We found no significant differences in triglyceride responses to PRO- and CHO + PRO-meal compared to the control-meal. However, the addition of casein to the CHO-meal reduced the raised triglyceride response in the chylomicron-rich fraction. Retinyl palmitate responses did not differ significantly between meals in the chylomicron-rich fraction, whereas the PRO-meal increased retinyl palmitate in the chylomicron-poor fraction. PRO- and PRO + CHO-meal increased insulin and glucagon compared to the control-meal. PRO + CHO-meal increased the glucose-dependent insulinotropic peptide response while no change in glucagon-like peptide-1 responses was detected. Conclusions: The data presented suggest that casein per se did not modulate the postprandial triglyceride response in type 2 diabetes. When added to carbohydrate, casein suppressed the triglyceride response in the chylomicron-rich fraction, increased insulin and glucagon but did not affect the incretin responses.

OriginalsprogEngelsk
TidsskriftNutrition, Metabolism & Cardiovascular Diseases
Vol/bind20
Udgave nummer2
Sider (fra-til)101-109
Antal sider9
ISSN0939-4753
DOI
StatusUdgivet - feb. 2010

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